ArticleCell death and differentiation2020
Deletion of heat shock protein 60 in adult mouse cardiomyocytes perturbs mitochondrial protein homeostasis and causes heart failure.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 114 citations in OpenAlex.
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- Driving proteomic imbalance in malignancy provokes proteomic catastrophe and confers tumor suppression.bioRxiv : the preprint server for biology · 2026Article
- Chaperonin in health and disease.Molecular biomedicine · 2026Review
- Dietary chromium picolinate-promoted oxidative phosphorylation may be a potential mean to improve hypoxia tolerance of juvenile grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Aberrant mitochondrial hsp60 expression affects mitochondria homeostasis and results in muscle dystrophy and premature death.Cell death & disease · 2026Article
- A Biochemical Analysis of LINC00896 RNA in Cortex Neuronal Cells and Its Possible Connection to the Development of Autism.Journal of nucleic acids · 2026Article
- Effects of Dominant Associated BacteriaMicroorganisms · 2025Article
- Mitochondrial quality control in cardiomyocytes: safeguarding the heart against disease and ageing.Nature reviews. Cardiology · 2025Review
- HSPA9/HMGB1 regulates myocardial fibrosis in atrial fibrillation via TGF-β1/Smad pathway and autophagy.Molecular biology reports · 2025Article
- Deletion ofJournal of developmental biology · 2025Article
- Modulation of Lonp1 Activity by Small Compounds.Biomolecules · 2025Review
- Depletion of HSP60 in Microglia Leads to Synaptic Dysfunction and Depression-Like Behaviors Through Enhanced Synaptic Pruning in Male Mice.CNS neuroscience & therapeutics · 2025Article
- α Protein Kinase 3 Is Essential for Neonatal and Adult Cardiac Function.Journal of the American Heart Association · 2025Article
- Mitochondrial fusion and cristae reorganization facilitate acquisition of cardiomyocyte identity during reprogramming of murine fibroblasts.Cell reports · 2025Article
- Macrophage-derived S100A9 promotes diabetic cardiomyopathy by disturbing mitochondrial quality control via STAT3 activation.International journal of biological sciences · 2025Article
- Oligomeric Proanthocyanidins Ameliorate Cadmium-Induced Senescence of Osteocytes Through Combating Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2024Article
- Loss of GATAD1 in cardiomyocyte does not cause cardiomyopathy in mice.Journal of molecular histology · 2024Article
- Aging of alveolar type 2 cells induced byBiomolecules & biomedicine · 2024Article
- Mammalian integrated stress responses in stressed organelles and their functions.Acta pharmacologica Sinica · 2024Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 5 institutions in 2 countries.
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Abstract
To maintain healthy mitochondrial enzyme content and function, mitochondria possess a complex protein quality control system, which is composed of different endogenous sets of chaperones and proteases. Heat shock protein 60 (HSP60) is one of these mitochondrial molecular chaperones and has been proposed to play a pivotal role in the regulation of protein folding and the prevention of protein aggregation. However, the physiological function of HSP60 in mammalian tissues is not fully understood. Here we generated an inducible cardiac-specific HSP60 knockout mouse model, and demonstrated that HSP60 deletion in adult mouse hearts altered mitochondrial complex activity, mitochondrial membrane potential, and ROS production, and eventually led to dilated cardiomyopathy, heart failure, and lethality. Proteomic analysis was performed in purified control and mutant mitochondria before mutant hearts developed obvious cardiac abnormalities, and revealed a list of mitochondrial-localized proteins that rely on HSP60 (HSP60-dependent) for correctly folding in mitochondria. We also utilized an in vitro system to assess the effects of HSP60 deletion on mitochondrial protein import and protein stability after import, and found that both HSP60-dependent and HSP60-independent mitochondrial proteins could be normally imported in mutant mitochondria. However, the former underwent degradation in mutant mitochondria after import, suggesting that the protein exhibited low stability in mutant mitochondria. Interestingly, the degradation could be almost fully rescued by a non-specific LONP1 and proteasome inhibitor, MG132, in mutant mitochondria. Therefore, our results demonstrated that HSP60 plays an essential role in maintaining normal cardiac morphology and function by regulating mitochondrial protein homeostasis and mitochondrial function.
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